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Karen L. Eskow Jaunarajs

Researcher at Binghamton University

Publications -  11
Citations -  607

Karen L. Eskow Jaunarajs is an academic researcher from Binghamton University. The author has contributed to research in topics: Abnormal involuntary movement & Agonist. The author has an hindex of 9, co-authored 10 publications receiving 543 citations.

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Local modulation of striatal glutamate efflux by serotonin 1A receptor stimulation in dyskinetic, hemiparkinsonian rats

TL;DR: Findings indicate a novel anti-dyskinetic mechanism of action for 5-HT(1A)R agonists with implications for the improved treatment of Parkinson's disease.
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Potential mechanisms underlying anxiety and depression in Parkinson's disease: consequences of l-DOPA treatment.

TL;DR: An overview of the clinical characteristics of affective disorders in Parkinson's disease, the utility of animal models for the study of anxiety and depression in PD, and potential mechanisms by which DA loss and subsequent l-DOPA therapy influence monoamine function and concomitant affective symptoms are discussed.
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Behavioral and neurochemical effects of chronic L-DOPA treatment on nonmotor sequelae in the hemiparkinsonian rat

TL;DR: The data suggest that chronic L-DOPA therapy in severely DA-lesioned rats does not improve nonmotor symptoms and may impair nondopaminergic processes, indicating that long-term L- DOPA therapy does not exert necessary neuroplastic changes for improving affect.
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Serotonin transporter inhibition attenuates L-DOPA-induced dyskinesia without compromising L-DOPA efficacy in hemi-parkinsonian rats

TL;DR: The present results support targeting serotonin transporters to improve Parkinson's disease treatment and provide further evidence for the role of the serotonin system in l‐DOPA’s effects.
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Role of the primary motor cortex in L-Dopa-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

TL;DR: An integral role for M1 in LID and its modulation by local 5-HT1AR is supported and continuous infusion into M1 at peak dyskinesia alleviated L-Dopa-induced AIMs.